Animal models for diisocyanate asthma: answers for lingering questions.

摘要: PURPOSE OF REVIEW Diisocyanates are the leading cause of occupational asthma, most commonly reported lung disease associated with workplace. Clinical studies have implicated immune system in pathogenesis but ethical and moral issues prevent mechanistic investigations humans. For this reason, development characterization animal models germane to further understanding diisocyanate asthma identify avenues for therapeutic intervention. This review will highlight important features existing experimental emphasis on new developments. RECENT FINDINGS Experimental demonstrated an immunological basis disease. Mice can be sensitized by dermal or respiratory exposure, suggesting that either exposure route may Recent findings show mice develop airway hyperreactivity inflammation, reflective human The transfer lymphocytes serum from clinical naive mice. Transgenic animals identified a role specific immunity, including involvement T-helper type 1/2 responses as well CD4 CD8 T cells asthma. shown sensitization occur through subchronic inhalation vapor-phase at levels low 20 ppb. SUMMARY progress using has been instrumental furthering current pathogenesis. demonstration murine model after sub-chronic relevant should provide opportunities more accurate risk assessment data.